Dietary Iron Levels Research Articles

The effect of different dietary iron levels on growth and hepatic iron concentration in juvenile gibel carp (Carassius auratus gibelio)

An 83-day growth trial was conducted using a flow-through system to examine the effects of different dietary iron levels on growth and hepatic iron concentration in juvenile gibel carp (Carassius auratus gibelio). Six purified diets supplemented with different levels of iron (0, 10, 30, 60, 100 and 200 mg kg−1) (as ferrous sulfate) were fed to triplicate groups of fish (initial weight 2.12 ± 0.00 g per fish). The results showed that the addition of iron to the basal diet did not significantly affect the specific growth rate (SGR), feed efficiency (FE), survival, red blood cell amount (RBC), hemoglobin content (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) or mean corpuscular hemoglobin concentration (MCHC). Hepatic iron concentration and hematocrit (Hct) were significantly influenced by dietary iron level (P < 0.05). On the basis of the iron concentration for the maintenance of optimum hepatic iron concentration and Hct, it was concluded that the dietary iron concentration of juvenile gibel carp should be not less than 202 mg Fe kg−1 diet.

Ferritin accumulation under iron scarcity in Drosophila iron cells

Ferritins are highly stable, multi-subunit protein complexes with iron-binding capacities that reach 4500 iron atoms per ferritin molecule. The strict dependence of cellular physiology on an adequate supply of iron cofactors has likely been a key driving force in the evolution of ferritins as iron storage molecules. The insect intestine has long been known to contain cells that are responsive to dietary iron levels and a specialized group of “iron cells” that always accumulate iron-loaded ferritin, even when no supplementary iron is added to the diet. Here, we further characterize ferritin localization in Drosophila melanogaster larvae raised under iron-enriched and iron-depleted conditions. High dietary iron intake results in ferritin accumulation in the anterior midgut, but also in garland (wreath) cells and in pericardial cells, which together filter the circulating hemolymph. Ferritin is also abundant in the brain, where levels remain unaltered following dietary iron chelation, a treatment that depletes ferritin from the aforementioned tissues. We attribute the stability of ferritin levels in the brain to the function of the blood-brain barrier that may shield this organ from systemic iron fluctuations. Most intriguingly, our dietary manipulations demonstrably iron-depleted the iron cells without a concomitant reduction in their production of ferritin. Therefore, insect iron cells may constitute an exception from the evolutionary norm with respect to iron-dependent ferritin regulation. It will be of interest to decipher both the physiological purpose served and the mechanism employed to untie ferritin regulation from cellular iron levels in this cell type.

Curcumin, a cancer chemopreventive and chemotherapeutic agent, is a biologically active iron chelator

AbstractCurcumin is a natural product currently in human clinical trials for a variety of neoplastic, preneoplastic, and inflammatory conditions. We previously observed that, in cultured cells, curcumin exhibits properties of an iron chelator. To test whether the chelator activity of curcumin is sufficient to induce iron deficiency in vivo, mice were placed on diets containing graded concentrations of both iron and curcumin for 26 weeks. Mice receiving the lowest level of dietary iron exhibited borderline iron deficiency, with reductions in spleen and liver iron, but little effect on hemoglobin, hematocrit, transferrin saturation, or plasma iron. Against this backdrop of subclinical iron deficiency, curcumin exerted profound 2 effects on systemic iron, inducing a dose-dependent decline in hematocrit, hemoglobin, serum iron, and transferrin saturation, the appearance of microcytic anisocytotic red blood cells, and decreases in spleen and liver iron content. Curcumin repressed synthesis of hepcidin, a peptide that plays a central role in regulation of systemic iron balance. These results demonstrate that curcumin has the potential to affect systemic iron metabolism, particularly in a setting of subclinical iron deficiency. This may affect the use of curcumin in patients with marginal iron stores or those exhibiting the anemia of cancer and chronic disease.

Iron and copper, and their interactions during development

During development, the fetus is entirely dependent on the mother for its nutrient requirements. Subsequently, it is a period when both are vulnerable to changes in dietary supply, especially of those nutrients that are marginal under normal circumstances. In developed countries, this applies mainly to micronutrients. Even now, iron deficiency is a common disorder, especially in pregnancy. Similarly, copper intake in the U.K. population is rarely above adequate levels. It is now becoming clear that nutrient deficiencies during pregnancy can result in problems for the offspring, in both the short- and long-term. Early studies showed that lambs born to mothers on copper-deficient pastures developed 'swayback', with neurological and muscular symptoms that could not be reversed by postnatal supplementation. Our own findings have shown that prenatal iron deficiency results in increased postnatal blood pressure, even though the offspring have normal dietary iron levels from birth. These observations emphasize the importance of iron and copper in growth and development. Complicating the situation further is the fact that copper and iron are known to interact with each other in many ways, including absorption and intracellular transport. However, their interactions during the pregnancy appear to be more complex than during the non-pregnant state. In the present review, we examine the importance of these metals and their interactions, the consequences, both short- and long-term, of deficiency and consider some possible mechanisms whereby these effects may be generated.

Effects of Dietary Iron Levels on Growth Performance, Hematological Status, Liver Mineral Concentration, Fecal Microflora, and Diarrhea Incidence in Weanling Pigs

An experiment was conducted in weanling pigs (Landrace x Yorkshire x Duroc) to evaluate the effects of dietary iron levels on growth performance, hematological status, liver mineral concentration, fecal microflora, and diarrhea incidence. One hundred and forty-four piglets (initial BW 5.96 +/- 0.93 kg) were randomly allotted to one of the four dietary treatments on the basis of their body weights. The basal diets for each phase (phase 1: days 0 to 14; phase 2: days 15 to 28) were formulated to contain minimal Fe and then supplemented with gradient levels of Fe (0, 50, 100, and 250 mg/kg) from ferrous sulfate. Feces were collected on days 14 and 28 and used for the analysis of microbial count and trace minerals. Eight piglets from each treatment (two piglets per pen) were bled at 0, 7, 14, 21, and 28 days to determine their hematological and plasma Fe status. In addition, two piglets from each pen (eight piglets per treatment) were killed at days 14 and 28 to determine liver mineral concentrations. Pigs fed supplemental 250 ppm Fe showed lowest overall average daily gain (linear, p = 0.036). Diarrhea incidence was linearly increased (p < 0.001) with supplemental Fe level. On days 14, coliform population in normal feces was increased (p = 0.036) linearly with supplemental Fe level, and there were higher (p = 0.043) coliform population and lower (p < 0.001) Bifidobacterium spp. in the diarrhea feces. Supplemental Fe linearly (p < 0.05) improved the total red blood cells, hemoglobin, plasma, and liver (p = 0.109) Fe status of pigs and also increased (linear and quadratic, p < 0.001) the fecal excretion of Fe on days 14 and 28. It is concluded that increasing the dietary iron levels in piglets improved their hematological status and liver Fe content; however, higher dietary Fe levels might also be associated with the increased diarrhea incidence.

GERMINAÇÃO DE SEMENTES ARMAZENADAS DE CUBIU SOB DIFERENTES CONDIÇÕES DE LUZ

O cubiu (Solanum sessiliflorum Dunal) é uma espécie nativa da região amazônica que tem se expandido além do seu centro de origem. A planta possui potencial para a agroindústria devido a alta produtividade de frutos e acúmulo de altos níveis de ferro, niacina e ácido cítrico. Atualmente, há grande quantidade de informações sobre suas características culinárias, nutricionais e medicinais. Por outro lado, são relativamente escassas informações sobre exigências quanto ao processo germinativo como, por exemplo, sobre a qualidade de luz, a qual tem grande influência na germinação de sementes de tamanho pequeno. Assim, o presente trabalho teve como objetivo avaliar o efeito de diferentes condições de luz sobre a germinação das sementes de S. sessiliflorum Dunal variedade ‘Santa Luzia’, acondicionadas em embalagem de papel Kraft e armazenadas em geladeira (± 4 ºC) por seis meses. Foram testadas quatro condições de luz: branca, vermelha, vermelha extrema e ausência de luz. A intensidade luminosa foi produzida por quatro lâmpadas fluorescentes (20 W) fixadas internamente na porta do germinador. As condições de luz foram obtidas através da cobertura, com papel celofane, de caixas do tipo gerbox, onde se procedeu a semeadura. Foram avaliadas as seguintes variáveis: porcentagem de germinação, índice de velocidade de germinação, comprimento e massa seca de plântulas. As sementes de cubiu germinaram em todas as condições de luz, entretanto maiores porcentagens de germinação, índice de velocidade de germinação e comprimento de plântulas ocorreram sob luz vermelha e vermelha extrema.

Growth, haematological parameters and tissue lipid peroxidation of soft-shelled turtles,Pelodiscus sinensis, fed diets supplemented with different levels of ferrous sulphate

Soft-shelled turtles, Pelodiscus sinensis, with an average weight of 5.55 g, were fed diets supplemented with eight levels of ferrous sulphate for 8 weeks. The analysed iron content ranged from 50.8 to 482.9 mg kg⁻¹. Growth rate of turtles fed the control diet with no iron supplementation was the lowest among all dietary groups. Haematological parameters including red blood cell, haemoglobin, haematocrit, mean corpuscular volume, mean corpuscular haemoglobin and mean corpuscular haemoglobin concentration of the turtles fed the control diet were also significantly (P < 0.05) lower relative to the other groups. Thus, dietary iron at 50.8 mg kg⁻¹ (no supplemented iron) was deemed deficient for growth and ineffective at preventing anaemia in juvenile soft-shelled turtle. Whereas, a supplementation of 50 mg kg⁻¹ ferrous sulphate (a total dietary iron of 91.8 mg kg⁻¹) was enough to normalize the haematological values of soft-shelled turtles to the level similar to other iron supplement-fed groups. Within the tested dietary iron range, liver iron content curve-linearly (r² = 0.99) increased with increasing dietary iron level. Furthermore, thiobarbituric acid-reactive substances in liver tissues of the turtles have also increased when liver iron content increased. The dietary iron requirement of soft-shelled turtle is 120-198 mg kg⁻¹ when ferrous sulphate is used as the source of iron.

Oxidative‐inflammatory damage in cirrhosis: Effect of vitamin E and a fermented papaya preparation

Oxidative DNA damage occurs as an early event in hepatitis C virus (HCV) infection and is an indication of the potential for carcinogenesis. The aim of this study was to test a novel antioxidant/immunomodulator in patients with HCV-related cirrhosis. The study group consisted of 50 patients with HCV-related cirrhosis with transaminase values less than twofold increased (alanine aminotransferase [ALT] < 80 IU/L). Patients underwent a standardized food-vitamin composition assessment and were assessed for dietary intake, nutritional status and iron level. Patients were randomly allocated into two groups and then given either alpha-tocopherol 900 IU/day or 9 g/day of a fermented papaya preparation (FPP, Immun-Age, Osato Research Institute, Gifu, Japan) at bedtime for 6 months. Ten healthy subjects served as controls. Patients were checked monthly for: routine tests, redox status (reduced glutathione, glutathione peroxidase, oxidized glutathione, malondialdehyde), plasma alpha-tocopherol, 8-hydroxy-deoxy-guanidine (8-OHdG) level in circulating leukocyte DNA and serum levels of cytokines. Patients with cirrhosis showed a significant imbalance of redox status (low antioxidants/high oxidative stress markers) (P < 0.005 vs controls). Neither treatment regimen affected transaminases as a whole. However, vitamin E supplementation almost normalized ALT only in the limited vitamin-E-deficient subgroup. A significant improvement of redox status was obtained by both regimens. However, only FPP significantly decreased 8-OHdG and the improvement of cytokine balance with FPP was significantly better than with vitamin E treatment (P < 0.05). Although the present data seem to suggest a potential supportive role of antioxidants/immunomodulators as FPP in HCV patients, more studies are needed to substantiate their effect on the natural history of the disease.

DIETARY IRON REQUIREMENT OF THE NILE TILAPIA, OREOCHROMIS NILOTICUS (L.) FINGERLINGS IN INTENSIVE FISH CULTURE

The objective of the present study was to determine the dietary iron requirement for the Nile tilapia, Oreochromis niloticus fmgerlings in intensive fish culture system. O. niloticus fmgerlings (25.36±0.11g) were stocked in fiberglass tanks (lm3) under water running system at a density of 40 fish/m3 with a feeding level of 3% of body weight. Six purified diets containing different iron levels (0, 200, 400, 800, 1200 &1600 mg Fe/ Kg) in a form of ferrous sulphate were tested on the Nile tilapia for 8 weeks. Results revealed that FBW and SGR were the highest (P<0,05) in the fish group fed on the diet supplemented with 1200mg Fe /Kg and the lowest were recorded in fish fed on the iron free diet. Each of K and FI were insignificantly affected by dietary iron levels. The lowest value of FCR was recorded for fish fed on 1200mg Fe/ Kg diet. The results of the present study revealed that, the group offish fed 1200-mg Fe /Kg diet had significantly(P<0.05) the highest value of average daily gain in weight PPV and ER. Red blood cell count, haemoglobin and haematocrit values were increased with increasing the level of iron and significantly affected by dietary iron levels. The highest value of MCH was recorded for fish fed 1200 mg Fe /Kg diet. The lowest values of RBCs, Hb, ,Hcts MCVr MCH and MCHC were recorded for fish fed on iron free diet. TotaL plasma proteins and plasma glucose values were not significantly affected by increasing dietary iron level, while plasma cholesterol increased significantly by increasing the level of iron in the diet. The results of the present study suggest that iron supplemented to the diet up to a level of

Effect of dietary iron concentrations on growth, hematological parameters, and lipid peroxidation of soft-shelled turtles, Pelodiscus sinensis

A feeding trial was conducted to evaluate the effects of dietary ferric citrate supplementation on the growth, hematological parameters, and lipid peroxidation of juvenile soft-shelled turtles, Pelodiscus sinensis. Juvenile soft-shelled turtles (mean initial body weight 5.06 g) were fed diets supplemented with 0, 50, 100, 150, 200, 250, 350 or 450 mg/kg diet as ferric citrate for 8 weeks. The analyzed dietary iron contents were 57.5, 103.6, 139.1, 162.8, 242.6, 280.8, 366.7, and 474.8 mg/kg for the diets supplemented with 0, 50, 100, 150, 200, 250, 350, and 450 mg iron/kg, respectively. Growth, feed conversion ratio, and protein efficiency ratio were lowest for the turtles fed the basal diet with no supplemental iron. Tissue iron content and hematological parameters including red blood cell counts (RBC), hemoglobin (Hb), hematocrit (Hct), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC) of the turtles fed basal diet were significantly ( P < 0.05) lower than other groups. Muscle proximate composition was not ( P > 0.05) affected by the dietary iron level. Thiobarbituric acid-reactive substances (TBARS) increased significantly in both muscle and liver tissues when dietary iron level reached 280 mg/kg. Regression modeling using tissue iron contents and hematological parameters as the dependent variables indicated that the optimal dietary iron requirement for soft-shelled turtles was approximately 266–325 mg/kg using ferric citrate as the dietary iron source.

The influence of high iron diet on rat lung manganese absorption

Individuals chronically exposed to manganese are at high risk for neurotoxic effects of this metal. A primary route of exposure is through respiration, although little is known about pulmonary uptake of metals or factors that modify this process. High dietary iron levels inversely affect intestinal uptake of manganese, and a major goal of this study was to determine if dietary iron loading could increase lung non-heme iron levels and alter manganese absorption. Rats were fed a high iron (1% carbonyl iron) or control diet for 4 weeks. Lung non-heme iron levels increased approximately 2-fold in rats fed the high iron diet. To determine if iron-loading affected manganese uptake, 54Mn was administered by intratracheal (it) instillation or intravenous (iv) injection for pharmacokinetic studies. 54Mn absorption from the lungs to the blood was lower in it-instilled rats fed the 1% carbonyl iron diet. Pharmacokinetics of iv-injected 54Mn revealed that the isotope was cleared more rapidly from the blood of iron-loaded rats. In situ analysis of divalent metal transporter-1 (DMT1) expression in lung detected mRNA in airway epithelium and bronchus-associated lymphatic tissue (BALT). Staining of the latter was significantly reduced in rats fed the high iron diet. In situ analysis of transferrin receptor (TfR) mRNA showed staining in BALT alone. These data demonstrate that manganese absorption from the lungs to the blood can be modified by iron status and the route of administration.

Histidine nutrition and genotype affect cataract development in Atlantic salmon, Salmo salar L.

The aim of this study was to investigate effects of dietary levels of histidine (His) and iron (Fe) on cataract development in two strains of Atlantic salmon monitored through parr-smolt transformation. Three experimental diets were fed: (i) a control diet (CD) with 110 mg kg(-1) Fe and 11.7 g kg(-1) His; (ii) CD supplemented with crystalline His to a level of 18 g kg(-1) (HD); and (iii) HD with added iron up to 220 mg kg(-1) (HID). A cross-over design, with two feeding periods was used. A 6-week freshwater (FW) period was followed by a 20-week period, of which the first three were in FW and the following 17 weeks in sea water (SW). Fish were sampled for weighing, cataract assessment and tissue analysis at five time points. Cataracts developed in all groups in SW, but scores were lower in those fed high His diets (P < 0.05). This effect was most pronounced when HD or HID was given in SW, but was also observed when these diets were given in FW only. Histidine supplementation had a positive effect on growth performance and feed conversion ratio (P < 0.05), whereas this did not occur when iron was added. Groups fed HD or HID had higher lens levels of His and N-acetyl histidine (NAH), the latter showing a marked increase post-smoltification (P < 0.05). The HD or HID groups also showed higher muscle concentrations of the His dipeptide anserine (P < 0.05). There was a strong genetic influence on cataract development in the CD groups (P < 0.001), not associated with tissue levels of His or NAH. The role of His and His-related compounds in cataractogenesis is discussed in relation to tissue buffering, osmoregulation and antioxidation.

Regulation of divalent metal transporter expression in human intestinal epithelial cells following exposure to non-haem iron

A number of regulatory factors including dietary iron levels can dramatically alter the expression of the intestinal iron transporter DMT1. Here we show that Caco-2 cells exposed to iron for 4 h exhibited a significant decrease in plasma membrane DMT1 protein, though total cellular DMT1 levels were unaltered. Following biotinylation of cell surface proteins, there was a significant increase in intracellular biotin-labelled DMT1 in iron-exposed cells. Furthermore, iron-treatment increased levels of DMT1 co-localised with LAMP1, suggesting that the initial response of intestinal epithelial cells to iron involves internalisation and targeting of DMT1 transporter protein towards a late endosomal/lysosomal compartment.

Increased Expression of Hypothalamic NADPH–Diaphorase Neurons in Mice with Iron Supplement

Iron deficiency is known as the most important nutritional problem in the world. The loss of appetite is a common characteristic of iron deficiency. Iron-containing heme is required as a cofactor for nitric oxide synthase (NOS) which produces nitric oxide (NO). NOS in the central nervous system has been suggested to regulate food intake. Hence, we examined the expression of hypothalamic NOS at various levels of dietary iron. ICR mice (n = 30) were randomly divided into three groups based on the level of dietary iron and fed experimental diets for 4 weeks: the normal-iron diet group (7 mg/kg diet, n = 10), the low-iron diet group (21 mg/kg diet, n = 10) and the high-iron diet group (42 mg/kg diet, n = 10). Expression of NOS in the paraventricular nucleus (PVN) and lateral hypothalamic area (LHA) of hypothalamus was examined by histochemistry for nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-diaphorase). The high-iron diet mice showed significantly higher staining intensity of NADPH-diaphorase-positive neurons in the PVN and LHA than the normal- and low-iron diet mice.

Interaction of dietary iron and vitamin A influences the performance of broilers

Avian broiler chickens (504, 1-day old) were randomly divided into 9 groups with 4 replicates per treatment, to investigate the influence of dietary Fe and vitamin A levels on production performance, immune competence, serum catalase activity, serum insulin concentration, and indicators of blood iron status such as haemoglobin concentration and red cell count. Supplemental levels were: 0, 30, and 60 mg iron/kg diet; 750, 1500, and 2700 IU vitamin A/kg diet. The results showed that the iron concentration in the basal diet was sufficient for nutritional requirements and that iron supplementation was not necessary. Dietary iron levels did not affected bodyweight gain and feed : gain (P &gt; 0.05) during the whole period, but influenced serum insulin concentration significantly (P &lt; 0.01), with serum insulin concentration reaching a peak for the treatment 60 mg iron/kg. The influence of dietary iron level on haemoglobin concentration and erythrocyte count was significant (P &lt; 0.05) from 0 to 4 weeks, and on erythrocyte count from 5 to 7 weeks. Different supplemental levels of vitamin A did not influence production performance and serum antibody titre to Newcastle Disease Virus, but the influence on blood T lymphocyte levels was significant (P &lt; 0.01). The treatment with 2700 IU vitamin A/kg resulted in lower feed : gain and higher blood T lymphocyte levels than other treatments. Dietary vitamin A levels influenced serum catalase activity significantly (P &lt; 0.01). Catalase activity was the highest when vitamin A supplemental level was 2700 IU/kg. Dietary vitamin A levels significantly affected erythrocyte count (P &lt; 0.01) but not haemoglobin concentration during the whole period. The interaction of iron and vitamin A significantly (P &lt; 0.05) influenced bodyweight gain, serum antibody titre to Newcastle Disease Virus, and blood T lymphocyte levels. The interaction of iron and vitamin A significantly (P &lt; 0.01) influenced serum catalase activity at the end of Week 7, haemoglobin concentration during the whole period, and erythrocyte count from 0 to 4 weeks.The haemoglobin concentration and erythrocyte count in the group with no Fe supplementation and 750 IU vitamin A/kg were lower than normal values. The complementary effect between iron and vitamin A improved haemoglobin concentration and erythrocyte count in broilers.

Dietary Iron Promotes Azoxymethane-Induced Colon Tumors in Mice

: There is accumulating evidence that high levels of dietary iron may play a role in colon carcinogenesis. We used a mouse model to investigate the impact of elevated dietary iron on incidence of aberrant crypt foci (ACF; a preneoplastic lesion) on tumor formation and on induction of oxidative stress. A/J mice were injected intraperitoneally, once a week for 6 weeks, with the colonotropic carcinogen, azoxymethane (AOM) or saline (vehicle controls). Following AOM or saline treatments, mice were placed on diets of high (3,000 ppm) and low (30 ppm) iron. Mice in each treatment group were sacrificed at 6 and 10 weeks following the final injection with AOM or saline. Colons were removed for subsequent histopathological analysis, which revealed average increases of 4.6 ± 1.3 vs. 10.4 ± 2.5 total tumors at 6 weeks and 30.75 ± 2.7 vs. 41.5 ± 4.4 total tumors at 10 weeks per AOM-treated mouse on low- and high-iron diets, respectively. There were no significant differences in incidence of ACF attributable to iron, although there was a trend toward greater crypt multiplicity per focus in mice on high-iron diets. Notably, no tumors were observed in mice receiving vehicle control injections in place of carcinogen, regardless of the level of dietary iron. These data suggest that iron exerts its effect at the stage of tumor promotion, but is not sufficient to initiate tumor formation. To learn more about mechanisms by which iron promotes tumor growth, colons were assayed for several biomarkers of oxidative stress [BOS; total F2-isoprostanes (F2-IsoPs), 15-F2t-isoprostanes (8-IsoPGF2αs), Isofurans (IsoFs), and 8-hydroxyguanosines (8-OH[d]Gs)], as well as iron absorption, programmed cell death, and cellular proliferation. Elevated PCNA and TUNEL staining of the colon epithelium revealed hyperproliferative and apoptotic responses to iron, while no significant differences between iron groups were observed in each of the BOS that were assayed. Our results suggest that, following carcinogen exposure, elevated dietary iron promotes the growth of tumors with altered cellular homeostasis through a mechanism that is independent of oxidative stress.

Globus pallidus: a target brain region for divalent metal accumulation associated with dietary iron deficiency

Recently, iron deficiency has been connected with a heterogeneous accumulation of manganese in the rat brain. The striatum is particularly vulnerable, for there is a significant negative correlation between accumulated manganese and γ-aminobutyric acid levels. The effect of dietary iron deficiency on the distribution of zinc and copper, two other divalent metals with essential neurobiological roles, is relatively unexplored. Thus, the primary goal of this study was to examine the effect of manipulating dietary iron and manganese levels on the concentrations of copper, iron, manganese and zinc in five rat brain regions as determined with inductively coupled plasma mass spectrometry analysis. Because divalent metal transporter has been implicated as a transporter of brain iron, manganese, and to a lesser extent zinc and copper, another goal of the study was to measure brain regional changes in transporter levels using Western blot analysis. As expected, there was a significant effect of iron deficiency ( P < 0.05) on decreasing iron concentrations in the cerebellum and caudate putamen; and increasing manganese concentrations in caudate putamen, globus pallidus and substantia nigra. Furthermore, there was a significant effect of iron deficiency ( P < 0.05) on increasing zinc concentration and a statistical trend ( P = 0.08) toward iron deficiency–induced copper accumulation in the globus pallidus. Transporter protein in all five regions increased due to iron deficiency compared to control levels ( P < 0.05); however, the globus pallidus and substantia nigra revealed the greatest increase. Therefore, the globus pallidus appears to be a target for divalent metal accumulation that is associated with dietary iron deficiency, potentially caused by increased transporter protein levels.

Successful Reduction of Hepatocellular Hemosiderin Content by Dietary Modification in Toco Toucans (Ramphastos toco) With Iron-Storage Disease

Abstract The purpose of this study was to determine whether a reduction in dietary iron concentration can result in significant decreases in hepatocellular hemosiderin content in toucans with iron-storage disease. We studied 2 adult toco toucans (Ramphastos toco) previously diagnosed with iron-storage disease. Liver biopsy specimens were taken before lowering dietary iron levels to <100 mg/kg on a dry-matter basis and taken again 8 months later. One bird died from airsacculitis at 12 months, and a postmortem specimen was also analyzed. Computerized image analysis of the specimens showed significant reductions (P < .001) in hepatocellular hemosiderin content over this period. Computerized image analysis is a valid means of quantifying relative iron content in serial liver biopsy specimens and can be used to monitor response to dietary iron reductions in birds with iron-storage disease. The significant relative reduction in hepatocellular iron content in these 2 toucans with iron-storage disease, in respons...

Globus pallidus: a target brain region for divalent metal accumulation associated with dietary iron deficiency

Recently, iron deficiency has been connected with a heterogeneous accumulation of manganese in the rat brain. The striatum is particularly vulnerable, for there is a significant negative correlation between accumulated manganese and γ-aminobutyric acid levels. The effect of dietary iron deficiency on the distribution of zinc and copper, two other divalent metals with essential neurobiological roles, is relatively unexplored. Thus, the primary goal of this study was to examine the effect of manipulating dietary iron and manganese levels on the concentrations of copper, iron, manganese and zinc in five rat brain regions as determined with inductively coupled plasma mass spectrometry analysis. Because divalent metal transporter has been implicated as a transporter of brain iron, manganese, and to a lesser extent zinc and copper, another goal of the study was to measure brain regional changes in transporter levels using Western blot analysis. As expected, there was a significant effect of iron deficiency ( P < 0.05) on decreasing iron concentrations in the cerebellum and caudate putamen; and increasing manganese concentrations in caudate putamen, globus pallidus and substantia nigra. Furthermore, there was a significant effect of iron deficiency ( P < 0.05) on increasing zinc concentration and a statistical trend ( P = 0.08) toward iron deficiency–induced copper accumulation in the globus pallidus. Transporter protein in all five regions increased due to iron deficiency compared to control levels ( P < 0.05); however, the globus pallidus and substantia nigra revealed the greatest increase. Therefore, the globus pallidus appears to be a target for divalent metal accumulation that is associated with dietary iron deficiency, potentially caused by increased transporter protein levels.

Dietary iron regulates hepatic hepcidin 1 and 2 mRNAs in mice

Recently discovered peptide-hepcidin (Hepc) may be a central player in the communication of iron body stores to the intestinal absorptive cells and thus involved in the maintenance of iron homeostasis. The aim of this study was to determine the effects of the level of dietary iron on Hepc gene expression in the liver. OF1 male mice were fed for 3 weeks either control diet (35 mg iron/kg diet), low-iron diet (1 mg iron/kg diet), or high-iron diet (500 mg iron/kg diet), and Hepc 1 and 2 mRNA abundance in the liver was assessed by reverse transcriptase-polymerase chain reaction (RT-PCR). Results clearly showed that Hepc gene expression is upregulated by high dietary iron and downregulated when the dietary iron level is low. Both Hepc 1 and Hepc 2 expression responds coordinately to dietary iron. This work provides additional evidence of the key role of Hepc in the regulation of iron homeostasis.